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排序方式: 共有665条查询结果,搜索用时 15 毫秒
1.
A New Approach to Percutaneous Subclavian Venipuncture to Avoid Lead Fracture or Central Venous Catheter Occlusion 总被引:5,自引:0,他引:5
JEAN E. MAGNEY DAVID H. STAPLIN DAVID M. FLYNN DAVID W. HUNTER 《Pacing and clinical electrophysiology : PACE》1993,16(11):2133-2142
Pacemaker and defibrillator leads and central venous catheters placed by commonly recommended techniques have been found to pass through the subclavius muscle, the costocaracoid ligament, or the costoclavicular ligament before entering veins medial to the first rib. Entrapment by these soft tissues subjects leads and catheters to stresses imposed by movements of the ipsilateral upper extremity. Accordingly, a new approach has been developed that introduces the lead or catheter into the subciavian vein near the lateral border of the first rib. This placement avoids soft tissue entrapment and may extend the longevity of leads and catheters. 相似文献
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PLANT MARTIN A.; BAGNALL GELLISSE; FOSTER JEAN 《Alcohol and alcoholism (Oxford, Oxfordshire)》1990,25(6):691-698
During 1988 and 1989 a survey was conducted of the drinkinghabits and alcohol-related beliefs of a national sample of teenagersin England. Data were obtained from 6,244 respondents virtuallyall aged 1416. Heavy drinkers were significantly morelikely to report drinking in a mixed sex group than were otherteenagers. They were also more likely than others to have drunkillegally in licensed premises, and were distinctive from otherteenagers in relation to their self-reported reasons for drinkingand their alcohol-related beliefs. 相似文献
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G.-J. WU W.-F. CHEN C.-S. SUNG Y.-H. JEAN C.-H. HUNG F.-A. CHEN M.-H. HSIEH Z.-H. WEN 《Acta anaesthesiologica Scandinavica》2009,53(1):55-60
Background: It has been proposed that the volatile anesthetic isoflurane induces neuroprotection and that the endogenous opioid peptide dynorphin induces neurocytotoxicity in cells. The levels of dynorphin are often significantly elevated in neuropathophysiological conditions, and dynorphin can directly induce toxicity. However, the neuroprotective effects of isoflurane on dynorphin-induced cytotoxicity are still unclear.
Methods: In order to determine the effect of isoflurane on dynorphin-induced cytotoxicity in neuronal cells, we have designed a device wherein cultured human neuroblastoma SH-SY5Y cells can be exposed to isoflurane. Fully differentiated SH-SY5Y cells were obtained by treating the cells with retinoic acid for 6 days. We examined SH-SY5Y cell survival, apoptosis, and antiapoptotic protein expression by cell viability, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling stain, and Western blot analysis, respectively.
Results: After 16 h of dynorphin (10 μM) treatment, the SH-SY5Y cells showed significant cytotoxicity, apoptosis, and downregulation of the antiapoptotic Bcl-2 protein expression. These effects of dynorphin were significantly inhibited by isoflurane exposure for 32 h [pretreatment for 16 h and posttreatment (after dynorphin treatment) for 16 h].
Conclusion: Thus, our results suggest that isoflurane exerts neuroprotective effects in the case of dynorphin-induced pathophysiological disruption. 相似文献
Methods: In order to determine the effect of isoflurane on dynorphin-induced cytotoxicity in neuronal cells, we have designed a device wherein cultured human neuroblastoma SH-SY5Y cells can be exposed to isoflurane. Fully differentiated SH-SY5Y cells were obtained by treating the cells with retinoic acid for 6 days. We examined SH-SY5Y cell survival, apoptosis, and antiapoptotic protein expression by cell viability, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling stain, and Western blot analysis, respectively.
Results: After 16 h of dynorphin (10 μM) treatment, the SH-SY5Y cells showed significant cytotoxicity, apoptosis, and downregulation of the antiapoptotic Bcl-2 protein expression. These effects of dynorphin were significantly inhibited by isoflurane exposure for 32 h [pretreatment for 16 h and posttreatment (after dynorphin treatment) for 16 h].
Conclusion: Thus, our results suggest that isoflurane exerts neuroprotective effects in the case of dynorphin-induced pathophysiological disruption. 相似文献
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目的 研究慢性阻塞性肺病(COPD)稳定期患者长期家庭无创正压通气(NIPPV)治疗的意义.方法 回顾性分析2006~2007年法国Croix Rousse医院住院随访的接受NIPPV治疗的COPD稳定期慢性呼吸衰竭患者46例,比较患者治疗前和治疗后1、3、6、12、24和36个月的动脉血气变化;治疗前和治疗后6、12、24和36个月的肺功能改变.结果 患者应用NIPPV 1、3、6、12、24和36个月后的PaCO2较使用前皆显著下降(P均<0.05);1、3、12和36个月后的PaO2较使用前都显著升高(P均<0.05);而6、12、24和36个月后的肺功能第一秒用力呼气容积/用力呼气肺活量(FEV1/FVC)、FEV1占预计值%和FVC指标无明显改善,无统计学差异.结论 COPD稳定期长期家庭NIPPV治疗可改善血气、呼吸困难、头痛症状和提高生活质量,但在改善肺功能、延长生存期和降低死亡率方面的作用还有待进一步证实. 相似文献
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Sotalol is a beta-blocking drug devoid of membrane stabilizing properties, as well as intrinsic sympathomimetic actions, or cardioselectivity. In addition, sotalol prolongs atrial and ventricular repolarization (Class III antiarrhythmic activity). It appears to have less myocardial depressant effect than other beta-blocking agents. Given orally, bioavailability of the drug reaches 100%. Sotalol's plasma half-life is 15 hours (range 7–18) and is dependent only on renal function. In clinical practice, it has been found effective in the suppression of nearly all supraventricular and ventricular dysrrhythmias except those related to prolonged ventricular repolarization. Most common adverse effects are dyspnea, bradycardia, and fatigue, which results in drug termination in 16% of the cases. Torsades de pointes usually associated with bradycardia and drug induced QTc prolongation has been reported in 1.9%–3.5% of the patients receiving sotalol. This complication may be reduced by limiting the dose (< 640 mg/day) especially in patients with impaired renal function. In addition hypokalemia must be avoided. To sum up, the combination of Class II and Class III effects may carry additional benefits. However, further studies are required to test such hypotheses. 相似文献
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In the present study, we investigated the influence of estrogen on 3H-noradrenaline (3H-NA) release induced in the oviductal isthmus by electrical stimulation, potassium and calcium. The fractional release of 3H-NA was measured in oviducts isolated from ovariectomized rabbits and from ovariectomized rabbits treated with estradiol cypionate, 70 μg/kg im 72 h before an experiment. Electrical field stimulation of the intramural nerves induced muscle contraction and augmented the release of labelled NA from the muscle. The 3H-NA release was reduced after estrogen treatment when reuptake of NA into the nerve terminals was blocked by desipramine, 10-6 M. Estrogen also reduced the 3H-NA release evoked by exposure of the oviducts to 121 mM KCI in the presence of calcium (2.5 mM) and in a high potassium, calcium-free medium upon the addition of 2.5 mM calcium. In the presence of desipramine a small fraction of 3H-NA was released in high potassium, calcium-free medium. This release was unaffected by estrogen. These results suggest that estrogen reduces the release of NA from the adrenergic nerves within the oviduct and that this action is exerted primarily on the calcium-dependent release. It therefore might be due to a reduction in the entry of calcium into the nerve terminal. 相似文献